与南海西边界流有关的区域海洋学进展

从动力学角度,回顾了与南海西部主流系及其涡旋研究有关的南海物理海洋学的进展.主要内容涉及南海西边界流漂流浮标观测、西边界流源区涡旋遥感观测、西边界流源区跨陆架交换、涡流相互作用、西边界流年际变化、西边界流区海气相互作用、南海贯穿流等方面的进展.西边界流是一个强流系,其与季节和年际变化相关的结构特征、变率及跟某些动力过程的关联有待研究.在西边界流变率、涡旋环流相互作用、海气过程以及南海贯穿流取得了以下成果:(1)利用漂流浮标观测样本对南海西边界环流进行分析,指出南海西边界表层环流在到达越南中部沿岸后伴随着流幅变窄的同时流速加强;探讨了南海北部环流变化机理,定量诊断南海西边界流北支冬季逆风流产生的动力机制;利用航次数据对18°n断面的经向地转流进行诊断,表明南海西边界流的经向输送年际变化明显;(2)结合航次观测数据,对2003/2004年冬季南海北部2个反气旋涡旋和2007年夏季18°n附近的3个反气旋涡旋进行研究,指出冬季2个涡旋产生后以罗斯贝(rOSSby)波速度(约0.1M/S)沿北部陆坡向西南方向传播,并初步揭示了南海西边界环流与夏季3个涡旋的相互作用;南海北部陆架区涡旋西南向传播最大(最大为0.09M/S),而越南以东海域涡动能(EkE)最大,这都说明涡旋活动与南海西边界流存在强的相互作用;(3)发现南海西边界流附近海表面温度(SST)强的季节内振荡特征,进一步研究表明此区域冬季SST季节内变化会使潜热季节内信号减弱20%;(4)探讨了南海贯穿流的长期变化特征以及与整个太平洋环流系统的相互关联.国家自然科学基金重点项目(40830851); 国家重点基础研究发展计划(2011CB403504); 中国科学院近海海洋观测研究网络——西沙南沙海洋观测研究站建设项目(KZCX2-EW-Y040)资

年轻学生对计算机操作界面的颜色偏好研究

以年轻学生作为被试,采用迫选法和主观评价法,考察了年轻学生对计算机操作界面的颜色偏好(包括背景色及其与前景色的搭配)。结果表明:1)蓝色、紫色、灰蓝色和青绿色比较适宜作为操作界面的背景色,其中蓝色是最受欢迎的颜色; 2)在以蓝色、紫色和灰蓝色作为背景色时,被试对前景色的偏好表现出一定的规律性,即以白色、黄色系和绿色系为主

神经调节素1β通过激活Sirt1信号通路抑制自噬改善大鼠脑缺血再灌注损伤研究 Neuregulin 1β Improves Cerebral Ischemia Reperfusion Injury by Inhibiting Autophagy via Sirt1 Signaling Pathway in Rats

目的 探讨神经调节素1β（neuregulin 1β，NRG1β）是否通过抑制自噬减轻大鼠大脑中动脉缺血再灌注（middle cerebral artery occlusion reperfusion，MCAO/R）损伤，以及对沉默信息调节因子1（silent information regulator protein 1，Sirt1）信号通路的影响。 方法 将210只健康雄性SD大鼠随机分为假手术组（Sham组）、模型组（MCAO/R组）、治疗组（NRG1β组）、激动剂组（SRT501组）、激动剂+治疗组（SRT501+NRG1β组）、抑制剂组（EX527组）和抑制剂+治疗组（EX527+NRG1β组），每组30只。采用改良线栓法建立MCAO/R模型，线栓由颈外动脉插入颈内动脉18～22 mm，堵塞左侧大脑中动脉起始部。缺血2 h后，缓慢拔出线栓，恢复脑血流22 h。EX527（5 mg/kg）、SRT501（100 mg/kg）于术前30 min腹腔注射，NRG1β（2 μg/kg）于拔出线栓后由微量注射器注入颈内动脉。脑缺血2 h、再灌注22 h后采用改良神经损伤严重程度评分（modified neurological severity score，mNSS）法评价各组大鼠的神经行为功能，采用2，3，5-氯化三苯基四氮唑（2，3，5-triphenyltetrazolium chloride，TTC）染色法计算大鼠脑梗死体积比例，苏木精-伊红染色观察神经元形态变化，免疫印迹（western blot，WB）和免疫荧光（immunofluorescence，IF）法分别检测额叶皮质缺血半暗带（ischemic penumbra，IP）区Sirt1、LC3、P62蛋白的表达和阳性细胞指数（positive cell index，PCI）。 结果 NRG1β组大鼠的mNSS[（10.0±0.8）分 vs.（12.8±0.6）分，P<0.001]和脑梗死体积比例[（23.78%±3.52%）vs.（40.24%±1.55%），P<0.001]均优于MCAO/R组，差异具有统计学意义；与MCAO/R组比较，NRG1β组、SRT501组、SRT501+NRG1β组mNSS均有不同程度下降、脑梗死体积比例缩小；各组中SRT501+NRG1β组mNSS最低、脑梗死体积比例最小，EX527组mNSS最高、脑梗死体积比例最大。苏木精-伊红染色显示，NRG1β组大鼠的神经元形态结构损伤较MCAO/R组、EX527组有所改善。WB结果显示，NRG1β组Sirt1表达[（0.81±0.01）vs.（0.67±0.02），P<0.001]和P62表达[（0.92±0.01）vs.（0.78±0.02），P<0.001]均高于MCAO/R组，LC3表达[（0.49±0.02）vs.（0.94±0.03），P<0.001]低于MCAO/R组。IF结果显示，NRG1β组Sirt1 PCI[（0.67±0.01）vs.（0.52±0.02），P<0.001]和P62 PCI[（0.52±0.02）vs.（0.37±0.01），P<0.001]均高于MCAO/R组，LC3 PCI[（0.38±0.01）vs.（0.50±0.01），P<0.001]低于MCAO/R组。WB和IF检测显示，Sirt1与P62表达趋势一致，NRG1β组、SRT501组与SRT501+NRG1β组表达高于MCAO/R组，各组中SRT501+NRG1β组表达最高、EX527组表达最低；LC3蛋白表达趋势与Sirt1、P62相反，在NRG1β组、SRT501组与SRT501+NRG1β组表达较MCAO/R组低；各组中SRT501+NRG1β组表达最低、EX527组表达最高。 结论 NRG1β可通过激活MCAO/R损伤大鼠Sirt1信号通路抑制自噬发挥神经保护作用。 Abstract: Objective To investigate whether neuregulin 1β (NRG1β) can alleviate middle cerebral artery occlusion reperfusion (MCAO/R) injury in rats by inhibiting autophagy, and whether this effect is mediated by the silent information regulator protein 1 (Sirt1) signaling pathway. Methods A total of 210 healthy male SD rats were randomly divided into sham group (sham group), model group (MCAO/R group), treatment group (NRG1β group), agonist group (SRT501 group) and agonist combined with treatment group (SRT501+NRG1β group), inhibitor group (EX527 group) and inhibitor combined with treatment group (EX527+NRG1β group), with 30 rats in each group. The MCAO/R model was established by the modified thread occlusion method to occlude the initial part of middle cerebral artery. After 2 hours of ischemia, cerebral blood flow was restored for 22 hours. EX527 (5 mg/kg) and SRT501 (100 mg/kg) were injected intraperitoneally 30 minutes before surgery, and NRG1β (2 μg/kg) was injected into the internal carotid artery with a microsyringe after restoration of reperfusion. Neurological behavioral function was evaluated by modified neurological severity score (mNSS) at 2 hours after cerebral ischemia and 22 hours after reperfusion. The proportion of cerebral infarction volume in rats was calculated by TTC staining. Morphological changes of neurons were observed by hematoxylin-eosin (HE) staining. The western blot (WB) and immunofluorescence (IF) were used to detect the expression of Sirt1, LC3 and P62 proteins in ischemic penumbra of the frontal cortex. Results The mNSS [(10.0±0.8) vs. (12.8±0.6), P<0.001] and TTC staining results [(23.78%±3.52%) vs. (40.24%±1.55%), P<0.001] in NRG1β group were better than those in MCAO/R group. Compared with MCAO/R group, mNSS in NRG1β group, SRT501 group, SRT501+NRG1β group all decreased in different degree, and the proportion of TTC-stained infarct volume reduced. The mNSS and the proportion of infarct volume were the lowest in SRT501+NRG1β group, while they were the highest in EX527 group among these groups. HE staining showed that the morphological and structural damage of neurons in NRG1β group improved compared with that in MCAO/R group and EX527 group. The WB results showed that the expression of Sirt1 [(0.81±0.01)vs. (0.67±0.02), P<0.001] and P62 [(0.92±0.01) vs. (0.78±0.02), P<0.001] in NRG1β group were higher than those in MCAO/R group, and the LC3 expression [(0.49±0.02) vs. (0.94±0.03), P<0.001] was lower than that in MCAO/R group. The IF results showed that Sirt1 positive cell index (PCI) [(0.67±0.01) vs. (0.52±0.02), P<0.001] and P62 PCI [(0.52±0.02) vs. (0.37±0.01), P<0.001] in NRG1β group were higher than those in MCAO/R group, and LC3 PCI [(0.38±0.01)vs. (0.50±0.01), P<0.001] was lower than that in MCAO/R group. The WB and IF results showed that the expression trend of Sirt1 and P62 was consistent as follows, their expression in NRG1β, SRT501 and SRT501+NRG1β groups were higher than that in MCAO/R group, with the highest expression in SRT501+NRG1β group and the lowest expression in EX527 group; the expression trend of LC3 protein was contrary to that of Sirt1 and P62, and the expression of LC3 protein in NRG1β, SRT501 and SRT501+ NRG1β groups were lower than that in MCAO/R group, with the lowest expression in SRT501+NRG1β group and the highest expression in EX527 group. Conclusions NRG1β plays a neuroprotective role in MCAO/R rats by activating Sirt1 signaling pathway to inhibit autophagy

JUNO Sensitivity on Proton Decay p→νˉK+p\to \bar\nu K^+ Searches

The Jiangmen Underground Neutrino Observatory (JUNO) is a large liquid scintillator detector designed to explore many topics in fundamental physics. In this paper, the potential on searching for proton decay in $p\to \bar\nu K^+$ mode with JUNO is investigated.The kaon and its decay particles feature a clear three-fold coincidence signature that results in a high efficiency for identification. Moreover, the excellent energy resolution of JUNO permits to suppress the sizable background caused by other delayed signals. Based on these advantages, the detection efficiency for the proton decay via $p\to \bar\nu K^+$ is 36.9% with a background level of 0.2 events after 10 years of data taking. The estimated sensitivity based on 200 kton-years exposure is $9.6 \times 10^{33}$ years, competitive with the current best limits on the proton lifetime in this channel

JUNO sensitivity on proton decay p → ν K + searches*

The Jiangmen Underground Neutrino Observatory (JUNO) is a large liquid scintillator detector designed to explore many topics in fundamental physics. In this study, the potential of searching for proton decay in the $p\to \bar{\nu} K^+$ mode with JUNO is investigated. The kaon and its decay particles feature a clear three-fold coincidence signature that results in a high efficiency for identification. Moreover, the excellent energy resolution of JUNO permits suppression of the sizable background caused by other delayed signals. Based on these advantages, the detection efficiency for the proton decay via $p\to \bar{\nu} K^+$ is 36.9% ± 4.9% with a background level of $0.2\pm 0.05({\rm syst})\pm$$0.2({\rm stat})$ events after 10 years of data collection. The estimated sensitivity based on 200 kton-years of exposure is $9.6 \times 10^{33}$ years, which is competitive with the current best limits on the proton lifetime in this channel and complements the use of different detection technologies